| Literature DB >> 17602956 |
Jian Wang1, Jocelyn Fields, Chunying Zhao, John Langer, Rajesh K Thimmulappa, Thomas W Kensler, Masayuki Yamamoto, Shyam Biswal, Sylvain Doré.
Abstract
Nrf2 is a key transcriptional factor for antioxidant response element (ARE)-regulated genes. While its beneficial role has been described for stroke, its contribution to intracerebral hemorrhage (ICH)-induced early brain injury remains to be determined. Using wild-type (WT) and Nrf2 knockout (Nrf2(-/-)) mice, the role of Nrf2 in ICH induced by intracerebral injection of collagenase was investigated. The results showed that injury volume was significantly larger in Nrf2(-/-) mice than in WT controls 24 h after induction of ICH (P<0.05), an outcome that correlated with neurological deficits. This exacerbation of brain injury in Nrf2(-/-) mice was also associated with an increase in leukocyte infiltration, production of reactive oxygen species, DNA damage, and cytochrome c release during the critical early phase of the post-ICH period. In combination, these results suggest that Nrf2 reduces ICH-induced early brain injury, possibly by providing protection against leukocyte-mediated free radical oxidative damage.Entities:
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Year: 2007 PMID： 17602956 PMCID： PMC2039918 DOI： 10.1016/j.freeradbiomed.2007.04.020
Source DB: PubMed Journal: Free Radic Biol Med ISSN： 0891-5849 Impact factor: 7.376